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Biomedical subjects

Tomotsugu Tabata

Publications and source records attributed to Tomotsugu Tabata.

At least 19 recordsLinked to original sources

Clinical features of mixed physiology of constriction and restriction: echocardiographic characteristics and clinical outcome.

AIMS: An entity of patients with mixed physiology of constriction and restriction has been reported, however, the characteristics of these patients have not been well documented. We evaluated the clinical features and the outcome of these patients. METHODS AND RESULTS: Study subjects consisted of 38 patients (57+/-14 years, 8 females, 30 males) who were diagnosed as having mixed physiology based on transthoracic and/or transesophageal echocardiography, MRI (or CT), cardiac catheterization, endomyocardial biopsy and/or surgical findings. Prior radiation therapy was the most frequent (50%) cause of mixed physiology followed by coronary artery bypass graft without prior radiation (24%) and heart transplantation (8%). The respiratory variation of peak early diastolic transmitral flow velocity by pulsed Doppler transesophageal echocardiography was 10.7% in patients with sinus rhythm and 18.1% in patients with atrial arrhythmia. Pericardial thickening was noted adjacent to the right-sided chambers in 19 patients, left-sided chambers in 10 patients, or both in 9 patients. All-cause 5-year mortality was 40% and unrelated to age, etiology, left ventricular systolic function and therapeutic course. There was a statistically significant difference (p<0.01) between the survival rates in patients with mixed physiology and in patients with pure constriction (n=125). CONCLUSIONS: Due to the high mortality in this disease, discrimination of the entity from the patients with pure constriction is mandatory. Transthoracic and transesophageal echocardiography are helpful noninvasive techniques in the diagnosis and the understanding of the physiology of patients with mixed constriction and restriction.

Adult↗

Giant flow reversal in pulmonary venous flow as a possible mechanism for asynchronous pacing-induced heart failure.

BACKGROUND: Mechanistic roles of the immediate increase in left atrial (LA) pressure in pacing-induced congestive heart failure have not been clearly understood. We evaluated the impact of asynchronous rapid ventricular pacing on LA hemodynamics in this model. METHODS: Transthoracic and transesophageal echocardiography and hemodynamic assessment were performed in 23 healthy mongrel dogs. Data were acquired before and 5 minutes after initiation of rapid right ventricular pacing (200/min). RESULTS: At 5 minutes after initiation of the pacing, giant pulmonary venous (PV) flow reversal (-76 cm/s) was observed in association with 1:1 ventriculoatrial conduction or complete atrioventricular dissociation. This giant PV flow reversal corresponded to an inappropriately timed atrial contraction, especially during systole. Cardiac output (3.21 vs 2.00 L/min, P < .001) was decreased corresponding to the decrease in the forward blood volumes as described by decrease in the Doppler left ventricular (LV) outflow (8.99 vs 4.73 cm, P < .0001), mitral inflow (6.89 vs 3.19 cm, P < .0001), and PV flow (14.15 vs 7.22 cm, P < .0001) velocity integrals. As a result, there was a marked elevation of the mean pulmonary capillary wedge (9.1 vs 17.1 mm Hg, P < .001) and LV end-diastolic (8.2 vs 17.4 mm Hg, P < .01) pressures leading to congestive heart failure. CONCLUSIONS: The giant PV flow reversal seen during asynchronous rapid right ventricular pacing corresponds to an inappropriate atrial contraction, immediately elevates LA pressure, and may initially promote congestive heart failure. The increase in LV end-diastolic pressure associated with decreased LV ejection fraction caused decrease in the LV filling volume leading to further increase in the LA pressure. This sustained marked elevation in the LA pressure and LV end-diastolic pressure could contribute to the heart failure process.

Animals↗

Left ventricular geometry and myocardial contractility in patients with essential hypertension evaluated by myocardial velocity profile.

BACKGROUND: Left ventricular (LV) systolic function in the hypertensive heart has been evaluated considering geometric differences. The maximal systolic myocardial velocity gradient (Gmax) obtained from myocardial velocity profile can evaluate regional myocardial contractility. The purpose of this study was to assess LV myocardial contractility in the hypertensive heart using Gmax regarding geometric differences. METHODS: The study included 93 patients with essential hypertension. Gmax was correlated with relative wall thickness and LV mass index. LV myocardial contractility was assessed by classifying patients into normal geometry, concentric remodeling (CR), eccentric hypertrophy, and concentric hypertrophy (CH). RESULTS: Gmax has shown significant negative relationship with LV end-diastolic dimension. LV end-diastolic dimension in CH and eccentric hypertrophy groups was significantly greater than that in normal geometry and CR groups (CH vs CR, 4.9 vs 4.2 cm, P < .001). LV mass index was significantly greater in CH and eccentric hypertrophy groups than in the other groups (CH vs CR, 196 vs 122 g/m2, P < .001). Although there was no difference in relative wall thickness between CH and CR groups, Gmax was significantly smaller in CH than in CR group (1.8 vs 2.8 s(-1), P < .05). CONCLUSIONS: In patients with essential hypertension, LV myocardial contractility worsened corresponding to increase in LV dimension with similar wall thickness. Gmax obtained from myocardial velocity profile detected depressed myocardial contractility in patients with increased LV dimension.

Female↗

Diagnosis of cardiac amyloidosis based on the myocardial velocity profile in the hypertrophied left ventricular wall.

The myocardial velocity profile (MVP), derived from color-coded tissue Doppler imaging (TDI), can identify transmural heterogeneity based on the physiology and pathology of the myocardium. This study sought to clarify whether the MVP can differentiate cardiac amyloidosis from other causes of left ventricular hypertrophy. We recorded the MVP and determined its myocardial velocity gradient (MVG) in the ventricular septum and left ventricular posterior wall using color-coded TDI in 10 patients with cardiac amyloidosis, in 25 patients with hypertensive hypertrophied left ventricular wall, in 25 patients with asymmetric septal hypertrophy of hypertrophic cardiomyopathy, and in 20 clinically normal controls. End-diastolic ventricular septal thickness was similar among the cardiac amyloidosis, hypertension, and hypertrophic cardiomyopathy groups. Percent systolic thickening of the ventricular septum and left ventricular posterior wall calculated from M-mode left ventricular echocardiograms was lower in the cardiac amyloidosis group than in the hypertension, hypertrophic cardiomyopathy, or control group. Peak MVGs during systole and early diastole were lowest in the cardiac amyloidosis group, followed, in order, by the control, hypertension, and hypertrophic cardiomyopathy groups. The systolic and early diastolic MVPs in the ventricular septum and left ventricular posterior wall showed a characteristic serrated pattern in all patients with cardiac amyloidosis, but not in any other patient groups. In conclusion, MVPs in the ventricular septum and left ventricular posterior wall show a distinctive serrated pattern that may be related to amyloid deposition in the myocardium. Myocardial tissue characterization using color-coded TDI provides diagnostic information in patients with cardiac amyloidosis.

Adult↗

Potential application of tissue Doppler imaging to assess regional left ventricular diastolic function in patients with hypertrophic cardiomyopathy: comparison with 123I-beta-methyl iodophenyl pentadecanoic acid myocardial scintigraphy.

BACKGROUND: Tissue Doppler imaging (TDI) has been utilized to evaluate left ventricular myocardial dysfunction in patients with hypertrophic cardiomyopathy (HCM); however, no clear explanation for the abnormality of TDI variables has been forthcoming. HYPOTHESIS: Peak negative myocardial velocity gradient (MVG) derived from TDI may correlate with a disorder of fatty acid metabolism in patients with HCM. METHODS: Tissue Doppler imaging and 123I-beta-methyl iodophenyl pentadecanoic acid (123I-BMIPP) myocardial scintigraphy were performed in 15 patients with asymmetric septal hypertrophy (mean age 47 +/- 18 years) and in 12 healthy controls (mean age 43 +/- 10 years). RESULTS: In early 123I-BMIPP images, accumulation defects were observed in the ventricular septum in 12 patients and in the posterior wall in 8 patients with HCM. Peak negative MVG in the ventricular septum (1.1 +/- 0.5 vs. 2.8 +/- 0.5, p < 0.0001) and posterior wall (5.2 +/- 1.4 vs. 6.7 +/- 0.8, p < 0.01 ) was significantly lower in the HCM group than in the controls; also, these parameters were significantly lower in patients with than in those without a defect in the region in question. The peak negative MVG in the ventricular septum and posterior wall correlated inversely with the washout rate in all subjects. CONCLUSIONS: Peak negative MVG according to TDI is related to disorder of fatty acid metabolism in the regional left ventricular myocardium of patients with HCM.

Cardiomyopathy, Hypertrophic↗

Losartan improves regional left ventricular systolic and diastolic function in patients with hypertension: accurate evaluation using a newly developed color-coded tissue doppler imaging technique.

BACKGROUND: Angiotensin II receptor antagonists have recently been accepted as antihypertensive therapy. Tissue Doppler imaging (TDI) has been developed as a noninvasive tool to assess quantitatively regional myocardial motion abnormalities. This study was designed to determine whether our newly developed technique of color-coded TDI may be a useful means of quantifying the improvement in regional left ventricular (LV) myocardial contractility and relaxation after treatment with losartan in patients with hypertension. METHODS AND RESULTS: Losartan (50 to 100 mg) was administered for 6 months to 37 previously untreated patients with essential hypertension. Averaged myocardial velocity profiles (MVPs) for color-coded TDI were recorded in the ventricular septum and LV posterior wall before and after treatment. Peak myocardial velocities and peak myocardial velocity gradients (MVGs) in the LV walls were determined during systole and early diastole. The plasma concentration of transforming growth factor (TGF)-beta1 also was measured in all patients. Blood pressure and plasma TGF-beta1 level decreased after initiation of losartan therapy. The LV mass index and LV meridional end-systolic wall stress also decreased after treatment with losartan. LV geometry changed from a pattern consistent with concentric hypertrophy to normal geometry in 10 patients and to a pattern consistent with concentric remodeling in 5 patients, and from concentric remodeling to normal geometry in 5 patients after treatment with losartan. The ratio of early to late diastolic filling for the transmitral flow velocity increased after losartan treatment. The peak systolic and early diastolic myocardial velocities and MVGs in the ventricular septum and LV posterior wall increased after treatment with losartan, although the values 6 months after treatment with losartan were still lower than those in normal individuals. There were good correlations between changes in plasma TGF-beta1 level and changes in systolic and early diastolic MVGs 6 months after losartan. However, there were no significant correlations between changes in the systolic blood pressure and LV end-systolic wall stress and changes in the TDI parameters. CONCLUSION: Losartan improves regional LV function in patients with hypertension. Our newly developed averaged MVP and MVG measurements may be useful for accurately evaluating regional LV myocardial contractility and relaxation in these patients.

Aged↗

Syncope upon swallowing caused by an esophageal hiatal hernia compressing the left atrium: a case report.

We describe a patient with syncope associated with swallowing. This syncope was caused by transient compression of the left atrium (LA) by an esophageal hiatal hernia. Two-dimensional echocardiography demonstrated a hyperechoic mass compressing the LA from the posterior. With air insufflation of the esophagus, compression of the LA by this hernia sac was seen to increase. Pulsed and color Doppler echocardiography revealed greatly decreased velocity of blood flowing into the LA and left ventricle (LV). Thus, marked compression of the LA by an esophageal hiatal hernia can cause syncope by impeding blood flow from the LA to the LV. Echocardiography proved highly useful in diagnosis.

Aged↗

A patient with sustained ventricular tachycardia: identification of a responder to amiodarone using signal-averaged electrocardiogram.

A 75-year-old man suffered sustained ventricular tachycardia with syncopal attack. Ventricular tachycardias appeared repeatedly, and an electrical defibrillator was used after an anti-arrhythmic drug, such as lidocaine or mexiletine, proved ineffective. The tachycardias had multiple origins, and the signal-averaged electrocardiogram (SAECG) showed ventricular late potential before the administration of amiodarone. After administration, the filtered QRS and duration of the late potential increased, but the recurrence of tachycardias was suppressed. The reason for this is thought to be that amiodarone blocked the sodium channel and delayed conduction, consequently blocking reentry, because amiodaron has antiarrhymic properties with a prolongation of refractoriness and minimal effect on conduction velocity in ventricular myocardium, and inhibits sympathetic activity, and blocks L-type calcium channel besides the depression of the fast sodium channel. In this case, SAECG predicted to some degree whether or not this patient's ventricular tachycardia would respond to amiodarone.

Aged↗

Determinants of LV diastolic function during atrial fibrillation: beat-to-beat analysis in acute dog experiments.

Left ventricular (LV) diastolic function during atrial fibrillation (AF) remains poorly understood due to the complex interaction of factors and beat-to-beat variability. The purpose of the present study was to elucidate the physiological determinants of beat-to-beat changes in LV diastolic function during AF. The RR intervals preceding a given cardiac beat were measured from the right ventricular electrogram in 12 healthy open-chest mongrel dogs during AF. Doppler echocardiography and LV pressure and volume beat-to-beat analyses were performed. The LV filling time (FT) and early diastolic mitral inflow velocity-time integral (E(vti)) were measured using the pulsed Doppler method. The LV end-diastolic volume (EDV), peak systolic LV pressure (LVP), minimum value of the first derivative of LV pressure curve (dP/dt(min)), and the time constant of LV pressure decay (tau) were evaluated with the use of a conductance catheter for 100 consecutive cardiac cycles. Beat-to-beat analysis revealed a cascade of important causal relations. LV-FT showed a significant positive linear relationship with E(vti) (r = 0.87). Importantly, there was a significant positive linear relationship between the RR interval and LV-EDV in the same cardiac beat (r = 0.53). Consequently, there was a positive linear relationship between LV-EDV and subsequent peak systolic LVP (r = 0.82). Furthermore, there were significant positive linear and negative curvilinear relationships between peak systolic LVP and dP/dt(min) (r = 0.95) and tau (r = -0.85), respectively, in the same cardiac beat. In addition, there was a significant negative curvilinear relationship between dP/dt(min) and tau (r = -0.86). We have concluded that the determinants of LV diastolic function in individual beats during AF depend strongly on the peak systolic LVP. This suggests that the major benefit of slower ventricular rate appears related to lengthening of LV filling interval, promoting subsequent higher peak systolic LVP and greater LV relaxation.

Animals↗

Pulmonary venous flow by doppler echocardiography: revisited 12 years later.

In 2003, pulmonary venous flow (PVF) evaluation by Doppler echocardiography is being used daily in clinical practice. Twelve years ago, we reviewed the potential uses of PVF in various conditions. Some of its important uses in cardiology have materialized, while others have not and have been supplanted by newer approaches. Current applications of measuring PVF have included: differentiating constrictive pericarditis from restriction, estimation of left ventricular (LV) filling pressures, evaluation of LV diastolic dysfunction and left atrial (LA) function, and grading the severity of mitral regurgitation (MR). However, there have been a number of controversies raised in the use of PVF profiles. Using transthoracic echocardiography, there may be technical issues in measuring the atrial reversal flow velocity. The use of PVF in the evaluation of the severity of MR is not always specific and can be affected by atrial fibrillation (AF) and elevated mean LA pressure. Mitral valvuloplasty and radiofrequency ablation for AF, which are the newer applications of PVF in monitoring invasive procedures, are mentioned. This article reviews the important clinical role of Doppler evaluation of PVF, discusses its limitations and pitfalls, and highlights its newer applications.

Catheter Ablation↗

Prognostic value of the atrial systolic mitral annular motion velocity in patients with left ventricular systolic dysfunction.

BACKGROUND: Transmitral flow velocity variables are powerful predictors of poor prognosis in patients with left ventricular (LV) systolic dysfunction. However, these variables may not accurately reflect the severity of pulmonary congestion. This study was designed to determine whether the peak atrial systolic mitral annular motion velocity (MA-Aw) measured by pulsed Doppler tissue imaging can predict cardiac death or hospitalization for worsening heart failure in patients with LV systolic dysfunction. METHODS: MA-Aw was recorded in 96 patients with LV systolic dysfunction who were followed up for 29 +/- 10 months. All patients underwent Doppler echocardiography on entry into the study, and cardiac catheterization was performed in 45 patients. Patients were divided into 3 groups on the basis of the ratio of early (E) to late (A) diastolic filling (E/A) of the transmitral flow velocity: group 1 (n=31; E/A < 1); group 2 (n=37; 1 < or = E/A < 2); and group 3 (n=28; E/A > or = 2). RESULTS: During follow-up, 36 patients (38%) died of cardiac causes and 34 (35%) were hospitalized for worsening heart failure. There were 2 cardiac deaths (6%) in group 1, 14 (39%) in group 2, and 20 (56%) in group 3. The MA-Aw correlated closely with the mean pulmonary capillary wedge pressure. Univariate Cox model analysis showed that MA-Aw < or = 5 cm/s was the most powerful predictor of cardiac death or hospitalization for worsening heart failure compared with clinical, hemodynamic, and the other echocardiographic variables. Furthermore, MA-Aw < or = 5 cm/s was clearly discernible as a good predictor of cardiac mortality on multivariate Cox model and as assessed by Kaplan-Meier method. CONCLUSION: The MA-Aw obtained by pulsed Doppler tissue imaging is a sensitive index of pulmonary congestion in patients with LV systolic dysfunction. It is a simple and noninvasive outcome measure and can be used to monitor treatment.

Blood Flow Velocity↗

An evaluation of the use of new Doppler methods for detecting longitudinal function abnormalities in a pacing-induced heart failure model.

BACKGROUND: Doppler tissue echocardiography and color M-mode Doppler flow propagation velocity have proven useful in evaluating cross-sections of patients with left ventricular (LV) dysfunction, but experience with serial changes is limited. PURPOSE AND METHODS: We tested their use by evaluating the temporal changes of LV function in a pacing-induced congestive heart failure model. Rapid ventricular pacing was initiated and maintained in 20 dogs for 4 weeks. Echocardiography was performed at baseline and weekly during brief pacing cessation. RESULTS: With rapid pacing, LV volume significantly increased and ejection fraction (57%-28%), stroke volume (37-18 mL), and mitral annulus systolic velocity (16.1-6.6 cm/s) by Doppler tissue echocardiography significantly decreased, with ejection fraction and mitral annulus systolic velocity closely correlated (r = 0.706, P <.0001). In contrast to the mitral inflow velocities, mitral annulus early diastolic velocity decreased steadily (12.3-7.3 cm/s) resulting in a dramatic decrease in mitral annulus early/late (1.22-0.57) diastolic velocity with no tendency toward pseudonormalization. The color M-mode Doppler flow propagation velocity also showed significant steady decrease (57-24 cm/s) throughout the pacing period. Multiple regression analysis chose mitral annulus systolic velocity (r = 0.895, P <.0001) and propagation velocity (r = 0.782, P <.0001) for the most important factor predicting LV systolic and diastolic function, respectively. CONCLUSIONS: Doppler tissue echocardiography and color M-mode Doppler flow could evaluate the serial deterioration in LV dysfunction throughout the pacing period. These were more useful in quantifying progressive LV dysfunction than conventional ehocardiographic techniques, and were probably relatively independent of preload. These techniques could be suitable for longitudinal evaluation in addition to the cross-sectional study.

Animals↗

Novel approach to the quantitation of regional left ventricular systolic and diastolic function using tissue Doppler imaging to create a myocardial velocity profile and gradient.

The myocardial velocity profile (MVP) and gradient (MVG) between the endocardium and epicardium of the left ventricular (LV) wall measured by color-coded tissue Doppler imaging (TDI) are new indices for evaluating regional LV myocardial function. However, accurate recording and measurement of the MVP is difficult using conventional methodology because of the stochastic nature of the ultrasound signal; that is, the effect of speckled noise. The aim of this study was to validate the accuracy and establish the validity of a newly developed method for measuring the MVP and MVG using 10 clinically normal controls and 10 patients with a hypertensive hypertrophied LV posterior wall. A non-isotropic, averaging algorithm was developed that was capable of obtaining a stable MVP (averaged MVP). Averaged MVP was recorded using parasternal, LV short-axis, color-coded TDI, placing regions of interest along the LV posterior wall with the reference point for angle-correction being at the center of LV contraction. The velocity from epicardium to endocardium within the region of interest was automatically angle-corrected to calculate the velocity component radially relative to the LV cavity and was spatially averaged along the circumference within the region of interest. Inter- and intraobserber variabilities of measurements were lower in the averaged MVP and MVG than in the conventional MVP and MVG. The correlation coefficients of the linear regression lines of systolic and early diastolic MVPs in the LV posterior wall were higher in all controls and hypertensive patients with the averaged method than with the conventional TDI procedures. The mean peak systolic and early diastolic MVGs were lower in the hypertensive group than in the controls. In conclusion, the newly developed averaged MVP provides a stable and reproducible index for the quantitative assessment of regional LV myocardial function.

Adult↗

Determinants of the development of mitral regurgitation in pacing-induced heart failure.

The pacing-induced heart failure model provides an opportunity to assess the structural and functional determinants of mitral regurgitation (MR) in dilated cardiomyopathy. This study aimed to evaluate MR to better understand the multitude of factors contributing to its development. Heart failure was induced by rapid ventricular pacing (230 beats/min) in 40 mongrel dogs. Left ventricular (LV) size and MR were evaluated echocardiographically. LV contractility was analyzed using a conductance catheter. MR increased to mild in 12 animals (regurgitant orifice area, 0.06+/-0.05 cm(2)), moderate in 15 (0.14+/-0.07 cm(2)), and severe in 13 (0.34+/-0.16 cm(2)). The grade of MR had an inverse relationships with E(max) (the slope of the end-systolic pressure-volume relationship, p<0.01) and dE/dt (the slope of the maximum rate of change of pressure-end-diastolic volume [V(ED)] relationship, p<0.01) and positive relationships with V(ED) and end-diastolic cross-sectional areas and lengths (p<0.05) by univariate analysis. The dE/dt had an independently significant (p<0.01) relationship by multivariable logistic regression. Many factors influence the development of MR and because of its similarity to the clinical situation, this model can be used to investigate MR and heart failure, as well as new surgical therapies.

Animals↗

Ventricular rate control by selective vagal stimulation is superior to rhythm regularization by atrioventricular nodal ablation and pacing during atrial fibrillation.

BACKGROUND: Selective atrioventricular nodal (AVN) vagal stimulation (AVN-VS) has emerged as a novel strategy for ventricular rate (VR) control in atrial fibrillation (AF). Although AVN-VS preserves the physiological ventricular activation sequence, the resulting rate is slow but irregular. In contrast, AVN ablation with pacemaker implantation produces retrograde activation (starting at the apex), with regular ventricular rhythm. We tested the hypothesis that, at comparable levels of VR slowing, AVN-VS provides hemodynamic benefits similar to those of ablation with pacemaker implantation. METHODS AND RESULTS: AVN-VS was delivered to the epicardial fat pad that projects parasympathetic nerve fibers to the AVN in 12 dogs during AF. A computer-controlled algorithm adjusted AVN-VS beat by beat to achieve a mean ventricular RR interval of 75%, 100%, 125%, or 150% of spontaneous sinus cycle length. The AVN was then ablated, and the right ventricular (RV) apex was paced either irregularly (i-RVP) using the RR intervals collected during AVN-VS or regularly (r-RVP) at the corresponding mean RR. The results indicated that all 3 strategies improved hemodynamics compared with AF. However, AVN-VS resulted in significantly better responses than either r-RVP or i-RVP. i-RVP resulted in worse hemodynamic responses than r-RVP. The differences among these modes became less significant when mean VR was slowed to 150% of sinus cycle length. CONCLUSIONS: AVN-VS can produce graded slowing of the VR during AF without destroying the AVN. It was hemodynamically superior to AVN ablation with either r-RVP or i-RVP, indicating that the benefits of preserving the physiological antegrade ventricular activation sequence outweigh the detrimental effect of irregularity.

Animals↗

Slow rate during AF improves ventricular performance by reducing sensitivity to cycle length irregularity.

Atrial fibrillation (AF) is characterized by short and irregular ventricular cycle lengths (VCL). While the beneficial effects of heart rate slowing (i.e., the prolongation of VCL) in AF are well recognized, little is known about the impact of irregularity. In 10 anesthetized dogs, R-R intervals, left ventricular (LV) pressure, and aortic flow were collected for >500 beats during fast AF and when the average VCL was prolonged to 75%, 100%, and 125% of the intrinsic sinus cycle length by selective atrioventricular (AV) nodal vagal stimulation. We used the ratio of the preceding and prepreceding R-R intervals (RR(p)/RR(pp)) as an index of cycle length irregularity and assessed its effects on the maximum LV power, the minimum of the first derivative of LV pressure, and the time constant of relaxation by using nonlinear fitting with monoexponential functions. During prolongation of VCL, there was a pronounced decrease in curvature with the formation of a plateau, indicating a lesser dependence on RR(p)/RR(pp). We conclude that prolongation of the VCL during AF reduces the sensitivity of the LV performance parameters to irregularity.

Animals↗

Nonexcitatory stimulus delivery improves left ventricular function in hearts with left bundle branch block.

INTRODUCTION: Preliminary data in a heart failure animal model and isolated muscle preparation have suggested that nonexcitatory stimulation (NES) improves left ventricular (LV) function. METHODS AND RESULTS: We compared biventricular (BV) pacing with NES in an animal model with left bundle branch block (LBBB). The left bundle branch (LBB) was ablated in eight normal heart pigs and led to >50% increase in QRS duration (mean 100 +/- 15 msec). End-diastolic LV pressure, end-systolic LV pressure, LV pressure (LV dP/dtmax), aortic pulse pressure, and LV ejection fraction were measured before pre-LBB ablation and compared with post-LBB ablation (AAI pacing), BV pacing, NES delivery, and BV+NES. Moreover, to evaluate LV diastolic function, we measured the early (E wave) and late flows (A wave) through the mitral valve using spectral Doppler. Compared with post-LBB ablation, NES led to a significant increase in LV dP/dtmax (1,047 +/- 224 mmHg/sec vs 897 +/- 116 mmHg/sec; P < 0.05), LV ejection fraction (64% +/- 18% vs 49% +/- 17%; P < 0.05), and aortic pulse pressure (18 +/- 3.6 mmHg vs 16 +/- 2.8 mmHg; P < 0.05). Moreover, improvement in LV hemodynamic parameters was significantly higher during NES delivery when compared with BV pacing. No significant changes in E wave, A wave, and E/A were recorded during NES, NES+BV, and BV pacing. CONCLUSION: Our preliminary data demonstrate that NES is superior to BV pacing in improving LV function in an animal model with LBBB. Moreover, we demonstrated that NES does not affect transmitral valve flow and subsequently LV diastolic function.

Animals↗

Early systolic mitral annular motion velocities responses to dobutamine infusion predict myocardial viability in patients with previous myocardial infarction.

OBJECTIVE: This study was undertaken for the determination of the correlation between myocardial viability and regional systolic mitral annular motion velocity (MAV) response to dobutamine stress in patients with previous myocardial infarction (MI) with pulsed tissue Doppler scan imaging. METHODS: The study included 45 patients (mean age, 65 +/- 12 years) with previous MI with 1 major coronary lesion and 30 healthy individuals (mean age, 61 +/- 14 years). 99mTc-methoxyisobutylisonitrile scintigraphy was performed to divide the patients into 2 groups: the viability (+) group (n = 25) and the viability (-) group (n = 20). Dobutamine was infused (at 2, 5, 10, and 20 microg/kg/min), and the peak first and second systolic MAVs (Sw1 and Sw2, respectively) were measured at the level of the mitral annulus corresponding to the infarct regions in the MI group and to the 6 mitral annular sites in the control group. In addition, the left ventricular wall motion score index (WMSI) was determined with 2-dimensional echocardiography. RESULTS: At baseline, the WMSI was significantly greater and the mean Sw1 and Sw2 were significantly lower in both the viability (+) and (-) groups than in the control group, but there were no significant differences between the viability (+) and (-) groups. After dobutamine infusion, the WMSI improved only in the viability (+) group. The mean Sw1 and Sw2 increased significantly with 2 microg/kg/min and 5 microg/kg/min of dobutamine, respectively, in the viability (+) group. With an increase in Sw1 of 2.0 cm/s or more with 5 microg/kg/min of dobutamine, viable myocardium was detected, with a sensitivity of 92% and a specificity of 90%. There were no significant increases in Sw1 or Sw2 in the viability (-) group with dobutamine infusion. CONCLUSION: Viable left ventricular myocardium is identified with peak early systolic MAV during dobutamine infusion.

Aged↗